>98%
Purity HPLC
COA
Every batch
EU
Fulfilment
Discreet
Shipping
>98%
Purity HPLC
COA
Every batch
EU
Fulfilment
Discreet
Shipping
NAD+ functions as an essential cofactor in hundreds of enzymatic reactions, most critically in the mitochondrial electron transport chain where it drives ATP synthesis. Its role extends beyond energy metabolism to include activation of sirtuins — a family of longevity-associated proteins — and PARP enzymes involved in DNA repair.
NAD+ levels decline significantly with age, a finding consistently associated with reduced mitochondrial function, increased oxidative stress, and impaired cellular repair capacity. Research into NAD+ precursors and direct supplementation has grown substantially over the past decade, driven by preclinical data demonstrating reversal of age-related metabolic decline in animal models.
Research has also documented NAD+’s role in circadian rhythm regulation, neurological function, and immune modulation, positioning it as one of the most broadly relevant compounds in longevity and metabolic research.
Key research areas include:
– Mitochondrial function and ATP synthesis
– Sirtuin activation and longevity pathways
– DNA repair via PARP activation
– Age-related metabolic decline
– Neurological function and neuroprotection
– Circadian rhythm regulation
- Mitochondrial Function
NAD+ is a critical electron carrier in the mitochondrial electron transport chain. Declining NAD+ levels are directly associated with reduced mitochondrial efficiency and increased production of reactive oxygen species in ageing tissue models. - Sirtuin Activation
NAD+ is an obligate substrate for sirtuin enzymes (SIRT1-7), which regulate gene expression, stress response, and metabolic adaptation. Preclinical studies have demonstrated that restoring NAD+ levels reactivates sirtuin-dependent longevity pathways. - DNA Repair
PARP enzymes, which consume NAD+ in the process of repairing DNA strand breaks, are critical for genomic stability. Research has documented that NAD+ availability is a rate-limiting factor in DNA repair efficiency, particularly under conditions of oxidative stress. - Age-Related Metabolic Decline
Animal studies have demonstrated that NAD+ restoration reverses multiple hallmarks of metabolic ageing, including mitochondrial dysfunction, reduced insulin sensitivity, and impaired muscle function, even when administered in aged subjects. - Neurological Function
Research has documented NAD+’s role in neuronal energy metabolism and its neuroprotective effects against excitotoxicity and oxidative damage, with implications for neurodegenerative disease models.
Key References:
– Yoshino J et al. NAD+ intermediates: the biology and therapeutic potential. Cell Metab. 2018.
– Verdin E. NAD+ in aging, metabolism, and neurodegeneration. Science. 2015.
– Rajman L et al. Therapeutic potential of NAD-boosting molecules. Cell Metab. 2018.- Mitochondrial Function
| Parameter | Detail |
| Peptide | NAD+ (Nicotinamide Adenine Dinucleotide) |
| Molecular Weight | 663.43 g/mol |
| CAS Number | 53-84-9 |
| Appearance | White lyophilised powder |
| Purity | >99% (HPLC) |
| Vial Size | 50mg |
| Storage | -20°C, protect from light and moisture |
| Reconstitution | Bacteriostatic water or sterile saline |
| Shelf Life | 24 months (lyophilised) / 30 days (reconstituted, refrigerated) |
| Format | Lyophilised powder, single-use research vial |
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